This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The acute respiratory distress syndrome (ARDS) is one of the most important causes for morbidity and mortality in intensive care medicine. It can be the sequel of diseases like sepsis, aspiration of gastric contents, pneumonia or trauma. It is characterized by an inflammatory reaction that leads to a breakdown of the alveolar-capillary barrier, resulting in an influx of fluid and proteins from the blood into the alveolar space. The exact mechanism of the inflammatory reaction is still incompletely understood. Numerous clinical and experimental trials have been made in order to improve the understanding and evaluate possible treatment options. It has been shown in clinical studies that the mode of mechanical ventilation, namely the tidal volume that is used, impacts survival of patients with this disease. The focus of our studies was on three different aspects: - The evaluation of pulmonary edema fluid samples of patients with ARDS compared to control samples - Induction of ventilator induced lung injury in rats and comparison of the proteome of alveolar type II cells from these animals with cells from not ventilated control animals - Induction of liver damage in rats by ischemia-reperfusion and evaluation of the proteome of the pulmonary alveolar type II cells to investigate the influence of a systemic inflammatory response on the proteome of these cells - In an additional project in cooperation with the UCSF liver center, proteomic changes in inflammatory cells were investigated. This was done using isolated Kupffer cells from rats with ischemia-reperfusion injury.